1.Study on the mechanism of Xiaoqinglong decoction in intervening in airway inflammation of asthma with syndrome of cold retention accumulation in lung
Bin WANG ; Mingzhe ZHAO ; Yuyang SUN ; Peizheng YAN
China Pharmacy 2025;36(13):1574-1580
OBJECTIVE To investigate the effects and potential mechanisms of Xiaoqinglong decoction on airway inflammation in asthma with syndrome of cold retention accumulation in lung based on the metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). METHODS Forty Wistar rats were randomly divided into blank group, model group, dexamethasone group (positive control, 1 mg/kg), and Xiaoqinglong decoction group (2.72 g/kg), with 10 rats in each group. A rat model of asthma with syndrome of cold retention accumulation in lung was established, and the corresponding drugs were administered once daily starting from the second day of modeling for 21 consecutive days. Lung histopathological changes and lung function were evaluated. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), interferron-γ (IFN-γ), tumor necrosis factor α (TNF-α), and interleukin-13 (IL-13) in serum were measured, and the mRNA expression levels of MALAT1, TNF- α, IL-13, IFN- γ, and transient receptor potential melastatin 2 (TRPM2) in lung tissue were determined. Twenty C57BL/6J wild-type mice and twenty C57BL/6J MALAT1(-/-)mice were randomly divided into wild-type model group, wild-type Xiaoqinglong decoction group, MALAT1 model group, and MALAT1(-/-) Xiaoqinglong decoction group, with 10 mice in each group. The same asthma model was E-mail:yan_peizheng@163.com established, and Xiaoqinglong decoction was administered once daily for 21 days starting from the second day of modeling. The serum levels of SOD, MDA, IFN-γ, TNF-α and IL-13 were measured, along with the mRNA and protein expression levels of TRPM2 in lung tissue. RESULTS The results of the rat experiment showed that, compared with model group, the airway resistance, functional residual capacity, the serum levels of IL- 13, TNF-α and MDA as well as inflammatory infiltration and collagen fiber deposition in lung tissue, and the expressions of IL- 13, TNF-α and TRPM2 in lung tissue were all significantly decreased in the treatment group (P<0.05 or P<0.01). The peak expiratory flow, forced expiratory flow at 50% of forced vital capacity, the serum levels of SOD and IFN-γ, and the expression levels of IFN-γ and MALAT1 in lung tissue were significantly increased (P<0.05 or P<0.01). The results of the mice experiment demonstrated that, compared with the wild-type model group, serum levels of IL-13, TNF-α and MDA in wild-type xiaoqinglong decoction group were significantly reduced (P<0.05 or P<0.01), while serum IFN-γ levels and SOD activity were significantly increased (P<0.01). Compared with the wild-type Xiaoqinglong decoction group, the MALAT1(-/-) Xiaoqinglong decoction group showed significantly decreased serum IFN-γ levels and SOD activity (P<0.01), along with significantly increased levels of IL-13, TNF-α and MDA (P<0.05 or P<0.01), as well as significantly elevated TRPM2 mRNA and protein expression in lung tissue (P<0.05). CONCLUSIONS Xiaoqinglong decoction may alleviate airway inflammation by regulating the expression of MALAT1, modulating oxidative stress, inhibiting TRPM2 activation, and reducing the release of pro-inflammatory cytokines.
2.Effects of Ephedra-Cinnamomum couplet medicinals on respiratory function and airway inflammation in rats with asthma of cold-fluid retention in lung syndrome and its mechanism
Mingzhe ZHAO ; Bin WANG ; Xiaomin ZHAO ; Yuyang SUN ; Peizheng YAN
China Pharmacy 2025;36(14):1717-1721
OBJECTIVE To investigate the effects of Ephedra-Cinnamomum couplet medicinals on respiratory function and airway inflammation in rats with asthma of cold-fluid retention in lung syndrome and its mechanism. METHODS Sixty Wistar rats were randomly divided into blank group, model group, dexamethasone group [1 mg/(kg·d)], and Ephedra-Cinnamomum low-, medium-, high-dose groups [0.234, 0.936, 1.872 g/(kg·d)], with 10 rats in each group. The model and treatment groups were sensitized by intraperitoneal injection of antigen solution (ovalbumin 100 mg + aluminum hydroxide 100 mg) and challenged with 1% ovalbumin nebulization, along with exposure to a cold environment and ingestion of cold water, to establish the asthma model with cold-fluid retention in lung syndrome. From day 2, rats received corresponding drugs or normal saline intragastrically, once a day, for 21 consecutive days. The general behavioral changes in each group of rats were observed during the experimental process. The lung function parameters [peak expiratory flow (PEF), airway resistance (Raw), functional residual capacity (FRC), expiratory flow at 50% of forced vital capacity (EF50%)] Δ 基金项目 国家自然科学基金青年科学基金项目(No.82004233); were measured before modeling and after the last medication as well as serum contents of interleukin-6 (IL-6), IL-13, tumor necrosis factor- α (TNF- α) and interferon-gamma (IFN- γ) after the last medication were determined; the histopathological morphological changes in the lung tissues of rats were also observed; mRNA expressions of IL-6, IL-3, TNF-α, IFN-γ, thymic stromal lymphopoietin (TSLP), and Toll-like receptor 4 (TLR4), as well as protein expressions of TSLP and TLR4 were determined in lung tissue. RESULTS Compared with model group, the lung tissue damage of rats was relieved significantly; Raw, FRC, the contents and mRNA expression levels of IL-6, IL-13 and TNF-α, as well as the mRNA and protein expressions of TSLP and TLR4 were significantly decreased (P<0.05), while the contents and mRNA expressions of PEF, EF50 % and IFN-γ were significantly increased in the dexamethasone group and Ephedra-Cinnamomum medium- and high-dose groups (P<0.05). Moreover, only a few rats in the two groups exhibited typical symptoms of asthma. CONCLUSIONS Ephedra-Cinnamomum couplet medicinals improve respiratory function and ameliorate airway inflammation in asthma rats with cold-fluid retention in lung syndrome, the mechanism of which may be associated with inhibiting TSLP/TLR4 signaling pathway and modulating Th1/Th2 imbalance.
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